Evidence map›Paper›PMID 28963462›Full record

ArticleScientific reports2017

Suppression of adiponectin receptor 1 promotes memory dysfunction and Alzheimer's disease-like pathologies.

Min Woo Kim, Noman Bin Abid, Myeong Hoon Jo, Min Gi Jo, Gwang Ho Yoon, Myeong Ok Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 3 pooled it
3.3field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 3 syntheses or guidelines pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. The role of adiponectin in Alzheimer's disease: A translational review.The journal of nutrition, health & aging · 2024
    Pooled it
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  16. Adiponectin rescues synaptic plasticity in the dentate gyrus of a mouse model of Fragile X Syndrome.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
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  17. Review
  18. The Role of Adipokines in the Pathologies of the Central Nervous System.International journal of molecular sciences · 2023
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Min Woo KimDivision of Life Science and Applied Life Science (BK 21 plus), College of Natural Sciences, Gyeongsang National University, Jinju, Republic of Korea.
Noman Bin AbidDivision of Life Science and Applied Life Science (BK 21 plus), College of Natural Sciences, Gyeongsang National University, Jinju, Republic of Korea.
Myeong Hoon JoDivision of Life Science and Applied Life Science (BK 21 plus), College of Natural Sciences, Gyeongsang National University, Jinju, Republic of Korea.
Min Gi JoDivision of Life Science and Applied Life Science (BK 21 plus), College of Natural Sciences, Gyeongsang National University, Jinju, Republic of Korea.
Gwang Ho YoonDivision of Life Science and Applied Life Science (BK 21 plus), College of Natural Sciences, Gyeongsang National University, Jinju, Republic of Korea.
Myeong Ok KimDivision of Life Science and Applied Life Science (BK 21 plus), College of Natural Sciences, Gyeongsang National University, Jinju, Republic of Korea. mokim@gnu.ac.kr.
Gyeongsang National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies on neurodegeneration have focused on dysfunction of CNS energy metabolism as well as proteinopathies. Adiponectin (ADPN), an adipocyte-derived hormone, plays a major role in the regulation of insulin sensitivity and glucose homeostasis in peripheral organs via adiponectin receptors. In spite of accumulating evidence that adiponectin has neuroprotective properties, the underlying role of adiponectin receptors has not been illuminated. Here, using gene therapy-mediated suppression with shRNA, we found that adiponectin receptor 1 (AdipoR1) suppression induces neurodegeneration as well as metabolic dysfunction. AdipoR1 knockdown mice exhibited increased body weight and abnormal plasma chemistry and also showed spatial learning and memory impairment in behavioural studies. Moreover, AdipoR1 suppression resulted in neurodegenerative phenotypes, diminished expression of the neuronal marker NeuN, and increased expression and activity of caspase 3. Furthermore, AD-like pathologies including insulin signalling dysfunction, abnormal protein aggregation and neuroinflammatory responses were highly exhibited in AdipoR1 knockdown groups, consistent with brain pathologies in ADPN knockout mice. Together, these results suggest that ADPN-AdipoR1 signalling has the potential to alleviate neurodegenerative diseases such as Alzheimer's diseases.

Indexed as

AdiponectinAlzheimer DiseaseAnimalsBody WeightCaspase 3Disease Models, AnimalDNA-Binding ProteinsGene Expression RegulationInsulinMaleMemory DisordersMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNuclear ProteinsAdiponectinadiponectin receptor 1, mouseAdipoq protein, mouseCasp3 protein, mouseCaspase 3DNA-Binding ProteinsInsulinNerve Tissue ProteinsNeuN protein, mouseNuclear ProteinsReceptors, AdiponectinRNA, Small Interfering

Identifiers

PMID28963462
PMCPMC5622055
OpenAlexW2757332320

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.